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Because of the anatomical and physiological differences
between fetal and adult circulations, the development
of heart failure in the fetus may follow slightly different
pathways than in the adult. In the adult alterations in
myocardial function, and subsequent decrease in cardiac
output, can be caused by alterations in one (or a
combination) of three basic mechanisms: (a) preload,
or ventricular filling pressure; (b) myocardial contractility
and heart rate; and (c) afterload or peripheral resistance
[1, 2]. Alterations in any of these mechanisms
can lead to decreased cardiac output and eventually to
cardiac failure.
In the fetus the development of chronic stress and
hypoxia results in alterations in fetal cardiovascular
function. Both animal experimentation and Doppler
evaluation of the human fetus have shown that
chronic stress causes an alteration in the right/left
heart dominance. During conditions of acute stress
the primary fetal response is increased fetal heart
rate. During conditions of chronic stress, however, alterations
in ventricular function lead to redistribution
of cardiac output and preferential perfusion of the fetal
brain and coronary arteries.
Rizzo et al. have postulated the theoretical response
of the fetal cardiovascular system to increasing
fetal stress: a decrease in fetal oxygenation or
substrate supply leads to a redistribution of cardiac
output, the so-called brain-sparing effect [14]. Eventually
the impairment of cardiac function causes an
increase in the atrioventricular gradient and an abnormal
cardiac filling which causes increased peripha
Chapter 35 Doppler Echocardiographic Assessment of Fetal Cardiac Failure 519
veins connect to this pathway. Blood flow in these
two pathways has the proximal inferior vena cava
in common but travels in different directions.
These anatomical and physiological relationships result
in different pathways for oxygenated and deoxygenated
blood returning to the fetal heart. Distal inferior
vena cava blood with low oxygen saturation
passes through pathway ªaº together with the right
hepatic venous flow and is directed into the right atria
where it joins the deoxygenated blood from the
superior vena cava and passes into the right ventricle.
Oxygenated blood from the umbilical vein passed
through the ductus venosus with some mixing with
blood from the left and medial hepatic veins and is
directed towards the foramen ovale and the left atria
and hence to the left ventricle. These studies in normal
human fetuses are, in the main, consistent with
previous studies in animal models.
The fetal anatomical shunt of the ductus arteriosus
allows the fetal heart to function in parallel rather than
in series, as in the adult heart [3]. The deoxygenated
blood from the superior vena cava and the ªaº pathway
blood from the inferior vena cava passes through the
tricuspid valve and is ejected out the pulmonary artery.
Because of the ductus arteriosus shunt, this poorly oxygenated
blood is directed into the descending aorta to
the lower carcass, and to the umbilical arteries for oxygenation
in the placental circulation. The left ventricle
outflow is directed through the ascending aorta to the
head and neck to supply the fetal brain with better oxygenated
blood derived primarily from the ªbº pathway
via the foramen ovale. In the normal fetus right ventricular
output is significantly greater than the left ventricular
output in a ratio of 1.3 to 1.
A detailed evaluation of cardiac anatomy should
always be undertaken in cases of suspected fetal heart
failure. Normally the two ventricles should be of relatively
similar size. Significant differences in ventricular
size can be related to structural anomalies (such
as hypoplastic left or right heart) or heart failure.
Cardiomegaly is a common finding in fetal heart failure.
Figure 35.5 shows cardiomegaly in a 24-week fetus
with both chronic and acute abruption. An evaluation
of cardiac size can be made by comparing the
anterior±posterior (AP) and transverse (trans.) diameters
of the thorax with the AP and the transverse diameters
of the heart in the axial view:
Ratio ˆ f‰ AP…
Hrt†‡Trans: … Hrt†
Š=2g=
f‰ AP…
Th†‡ Trans: … Th†
Š=2g
This ratio ranges from 45% to 55% and is independent
of gestational age [10]. Using M-mode, measurements
of the pulmonary and aortic root diameters
Fig. 35.5. Cardiomegaly in a 24-week fetus with acute and
chronic abruption
can be obtained. Deng et al. have shown a consistent
ratio between the pulmonary and aortic diameters of
1.09 (SD=0.06) with 5th and 95th percentile values of
1.06 and 1.11, respectively [11±13].
Fetal Cardiac Response to Stress